New Findings What is the topic of this review?The aim of this systematic review was to evaluate and summarize all published literature examining the impact of various exercise training interventions on endothelial function in postmenopausal women. What advances does it highlight?There was a moderate effect of training on macrovascular and microvascular endothelial function and just under two‐thirds of studies demonstrated a significant increase in at least one measure of endothelial function in postmenopausal women. Factors including exercise intensity and duration, vessel type, clinical status, hormone therapy, and menopausal status may influence the effects of training on endothelial function in postmenopausal women. Abstract Women experience a rapid decline in endothelial function during menopause. Therefore, it is important to explore interventions, such as exercise training, that may prevent endothelial dysfunction in postmenopausal women. The aim of this systematic review was to evaluate and summarize all published literature examining the impact of various exercise training interventions on endothelial function in postmenopausal women. Three electronic databases (MEDLINE, EMBASE and Web of Science) were used to systematically select studies related to exercise training, endothelial function and postmenopausal women. The major initial and secondary update systematic searches yielded 502 unique articles that were screened for eligibility. Thirty‐five studies were included in the systematic review. Two‐thirds of all studies demonstrated a group‐level increase in at least one measure of endothelial function with training. Most studies investigating biomarkers of endothelial function showed improvement in at least one measured biomarker post‐training. There was a moderate effect of training on both macrovascular and microvascular endothelial function in observational and randomized intervention studies. Variability in study designs, training protocols and participant characteristics make it difficult to directly compare studies. Factors including exercise intensity and duration, vessel type, clinical status, hormone therapy, and menopausal status may contribute to the inconsistent effects of training on endothelial function in postmenopausal women. Future research is needed in this population to understand the mechanisms driving inter‐study and inter‐individual differences in training‐induced changes in endothelial function.

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Several studies have demonstrated the relationship between acute changes in blood pressure and arterial stiffness utilizing perturbations that alter sympathetic nervous activity (SNA), which influences vascular tone. The purpose of the current study was to elicit changes in blood pressure without altering SNA to thus observe the isolated influence of local changes in blood pressure on arterial stiffness. In this scenario, myogenic responses and changes in elastic reserve may contribute to changes in stiffness. Eleven young and healthy adults (age 20± 2 years) participated in this study. Left forearm blood pressure was acutely manipulated by elevating the forearm above heart level (AHL; reduced blood pressure) or lowering the forearm below heart level (BHL; increased blood pressure). Using applanation tonometry at the wrist and antecubital fossa, arterial stiffness was assessed via pulse wave velocity (PWV) after 5 min of rest in three positions: heart level (HL), AHL and BHL. To determine myogenic response involvement, forearm vascular conductance (VC; forearm blood flow/forearm mean blood pressure) was also assessed with duplex ultrasound. Results are mean ± SD. Forearm mean blood pressure was significantly different between arm positions (p<0.001): BHL 99 ± 6 mmHg; HL 80 ± 5 mmHg; AHL 60 ± 4 mmHg. PWV was higher in the BHL (13.4 ± 7.6 m/s) and HL (10.8 ± 4.5 m/s) positions compared to the AHL position (7.4 ± 3.6 m/s) (p<0.001 and 0.01 respectively). Including all positions, blood pressure and PWV were positively correlated (r2=0.4, p=0.002). Forearm VC was significantly lower in the BHL position compared to the HL and AHL positions (p=0.002 and 0.001 respectively). AHL and HL VC were not significantly different (p=1.0). There was no correlation between PWV and VC (r2=0.04, p=0.78). In conclusion, these results indicate that increasing blood pressure results in increases in local arterial stiffness, independent of changes in SNA. The absence of correlation between VC and PWV suggests that changes in elastic reserve played a larger role than myogenic tone in determining changes in stiffness with acutely altered forearm blood pressure.

Conduit artery endothelial function is most commonly assessed via measurement of flow mediated dilation (FMD) evoked by a transient post‐limb occlusion increase in shear stress [reactive hyperemia (RH)]. A limitation of RH‐FMD is the uncontrolled nature of the RH shear stress stimulus which produces RH‐FMD response variability that is independent of conduit artery endothelial function. The purpose of this study was to develop a protocol to create a uniform, targeted, and transient (40 second) shear stress stimulus and compare it to the standard RH‐FMD approach. We hypothesize that incorporating arterial compression in the controlled targeted RH (CTRH) protocol will allow us to achieve a uniform target shear rate (estimate of shear stress) within and between participants. Young, healthy men and women (females n = 4, age = 22 ± 1 years; males n = 2, age = 25 ± 3 years) underwent one trial of RH‐FMD and two trials of CTRH‐FMD with duplex ultrasound assessment. The CTRH protocol incorporated three‐minutes of ischemic handgrip exercise at 30% of participants’ maximum voluntary contraction during a five‐minute occlusion to create a large forearm vasodilation and hyperemic reserve. Upon cuff release, the ensuing hyperemia was controlled with manual brachial artery compression at the antecubital fossa. A live velocity readout permitted compression adjustments to achieve the velocity required to maintain a target shear rate of 120 s‐1. The cuff was re‐inflated after 40s of cuff release. The RH‐FMD trial followed the standard five‐minute forearm occlusion protocol. The 40s average shear rate was 116.0 ± 8.8s‐1 in the CTRH test and 102.1 ± 15.4 s‐1 in the RH test. The CTRH test shear rate was significantly closer to the 120s‐1 target; calculated as the absolute distance from target in 3s time bins over the 40s period: CTRH = 19.0 ± 3.9s‐1; RH = 36.5 ± 6.7 s‐1 p = 0.002. The between participant coefficient of variation (CV) for the RH 40s average shear rate was lower in the CTRH test (CTRH CV = 8.1%; RH CV = 15.1%). The within subject trial to trial CV for the CTRH 40s average shear rate was 3.0 ± 4.6%. FMD responses were similar between tests (CTRH‐FMD% = 8.3 ± 1.6%; RH‐FMD% = 7.6 ± 4.8%, p=0.717). These preliminary findings demonstrate the capacity for RH stimulus control. CTRH‐FMD is minimally impacted by stimulus variability and may provide a clearer reflection of brachial artery endothelial function.